The purpose of this research is to continue the study of the pathophysiology of the various clinical syndromes which occur following glomerular injury using animal models of renal disease. This laboratory has for the past 2 years studied glomerular hemodynamics, tubular sodium reabsorption and filtration of macromolecules in a rat model of glomerulonephritis. We now propose to study other models of glomerular injury in rats as well. There are four main areas of interest: (1) Mechanisms for the adaptive restoration or maintenance of GFR following glomerular injury and reduction of ultrafiltration coefficient. (2) Study of distal nephron sodium and potassium handling in glomerulonephritis and the homeostatic action of aldosterone. (3) Mechanisms for hypertension following glomerular injury, in particular the role of the J-G apparatus and renin-angiotensin system as studied by assay of plasma and renal tissue for renin and by histologic and electron micrograph techniques. (4) A continued and more extensive study of macromolecular filtration in various models of glomerular injury.